Effects of FSTL1 on the proliferation and motility of breast cancer cells and vascular endothelial cells.

Abstract

BackgroundTreatments that prevent the motility of breast cancer cells and inhibit formation of new capillary vessels are urgently needed. FSTL1 is a secreted protein that has been implicated in maintaining the normal physiological function of the cardiovascular system, in addition to a variety of other biological functions. We investigated the role of FSTL1 in the proliferation and migration of breast cancer and vascular endothelial cells.MethodsHuman umbilical vein endothelial cells and human breast cancer BT‐549 cells were used to test the effects of FSTL1 and the N‐terminal domain of FSTL1. Immunofluorescence microscopy and 3‐(4, 5‐dimethylthiazolyl‐2)‐2,5‐diphenyltetrazolium bromide, transwell invasion, and wound healing assays were conducted.ResultsDifferent doses of the N‐terminal fragment of FSTL1 (FSTL‐N) have variable effects on the migration of these cells. However, FSTL1 does not significantly affect tube formation in vitro from vascular endothelial cells. FSTL1‐FL and FSTL1‐N have modest effects on the invasion of breast cancer and vascular endothelial cells. Interestingly, FSTL1‐FL, but not FSTL‐N, modulates vascular endothelial cell polarization.Conclusion FSTL1 modestly affects the proliferation of breast cancer cells and vascular endothelial cells. Our findings improve our understanding of the functions of FSTL1 in breast cancer development and angiogenesis.